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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Syntaxin 1A interacts with multiple exocytic proteins to regulate neurotransmitter release in vivo.

Biochemical studies suggest that syntaxin 1A participates in multiple protein-protein interactions in the synaptic terminal, but the in vivo significance of these interactions is poorly understood. We used a targeted mutagenesis approach to eliminate specific syntaxin binding interactions and demonstrate that Drosophila syntaxin 1A plays multiple regulatory roles in neurotransmission in vivo. Syntaxin mutations that eliminate ROP/Munc-18 binding display increased neurotransmitter release, suggesting that ROP inhibits neurosecretion through its interaction with syntaxin. Syntaxin mutations that block Ca2+ channel binding also cause an increase in neurotransmitter release, suggesting that syntaxin normally functions in inhibiting Ca2+ channel opening. Additionally, we identify and characterize a syntaxin Ca2+ effector domain, which may spatially organize the Ca2+ channel, cysteine string protein, and synaptotagmin for effective excitation-secretion coupling in the presynaptic terminal.[1]


  1. Syntaxin 1A interacts with multiple exocytic proteins to regulate neurotransmitter release in vivo. Wu, M.N., Fergestad, T., Lloyd, T.E., He, Y., Broadie, K., Bellen, H.J. Neuron (1999) [Pubmed]
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